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Tuesday, December 9, 2014

A new study reveals just how profoundly misled we are
about Bisphenol A and its analogs: they are at least 100x more toxic
than we previously imagined.

An alarming new study establishes that the commonly used chemical bisphenol A used in tens of thousands of consumer products, and its lesser known but increasingly prevalent analogs, bisphenol S
and F, are several orders of magnitude more disruptive to the endocrine
systems of the developing male human fetus than previous toxicological
risk assessments were capable of determining.

The
new study employed an innovative 'organotypic culture' system that took
tissue samples from mouse, rat and human fetal testis, in order to
create an experimental model that would accurately reproduce some of the
dynamics observable within in vivo (living organism-based) systems that are not ascertainable within conventional in vitro (cell-based) models. They termed this experimental environment the fetal testis assay (FeTA) system.

Disturbingly, they found:

"With
the use of a culture system that we developed (fetal testis assay
[FeTA]), we previously showed that 10 nmol/L BPA reduces basal
testosterone secretion of human fetal testis explants and that the
susceptibility to BPA is at least 100-fold lower in rat and mouse fetal testes." [emphasis added]

In
other word, the endocrine-disruptive effect of bisphenol A –
particularly its ability to suppress the testosterone-mediated
mascularization process during embryogenesis -- may be at least 100 times more toxic than previously believed.

How so?

Conventional
toxicological risk assessments of novel new chemicals like bisphenol A
are invariably performed on rodents, with effects (lethal dose 50%/LD50)
extrapolated to humans based merely on body weight differences. What
these do not account for is the contrasting ontological differences between cells of different species.
Nor do these acute lethal response studies (LD50) account for the
non-linear response between dose and effect (i.e. monotonicity).

An
accumulating body of scientific evidence has forced an acknowledgment
today that the low-dose effects of chemicals on hormonal systems include
the following counterintuitive response: a lower dose may have more profoundly disruptive effects on our hormonal system than higher doses.

This
concept may be so counterintuitive, that it begs for deeper
explanation. For instance, if chemical compound X at 1 milligram induces
programmed cell death within an exposed cell, and .01 milligram of
compound X induces a phenotypal change in the cell consistent with
cancer, it will be the latter effect (the lower dose) that may be more
detrimental in the long term, as cell death follows with stem-cell
mediated replacement of the damaged differentiated cell; whereas
chemically-induced carcinogenesis may result in the death of the entire
organism).

Case in point:

"Using the FeTA
system, we previously reported that basal testosterone secretion by
human testes was not affected by 10,000 nmol/L DES, but it was reduced
by concentrations as low as 10 nmol/L of BPA. Conversely, 10 nmol/L and
100 nmol/L BPA did not affect testosterone secretion by both mouse and
rat testes, and 10,000 nmol/L BPA was needed to observe a significant
reduction (58)."

The researchers also noted that
during the development of the nascent male human in embryogenesis
exposure to bisphenols in the 6.5th and 14th gestational weeks – the
window known to be critical for what is known as the ''masculinization
programming window' – these chemicals are likely contributing to the
alarming worldwide increase in male reproductive disorders, such as such
as "hypospadias [abnormally placed urinary hole], cryptorchidism [the
absence of one or both of the testicles], incomplete development or
agenesis of prostate and seminal vesicles, and reduction of the
anogenital distance (AGD) [ the distance from the anus to the genitalia]
and penis length."

Clearly, conventional toxicology, where the assumption is that a
higher concentration of a toxic substance is linearly connected to a
higher quantifiable adverse response, is no longer realistic. Living
systems are highly dynamic and complex and one can never predict how a
xenobiotic chemical will affect it. Any biologically incompatible
chemical, introduced at a critically important developmental window,
could result in untold adverse effects. The point is to eliminate
unnecessary exposures, instead of abiding by what regulators consider
'an acceptable level of harm.'

Clearly, the time is now to call
for a ban of bisphenol containing products. While 3.4 millions tons are
produced annually, with 20% of this being used as epoxy resin to coat
food and beverage metallic cans, we can no longer pretend, given the
latest research, that this chemical is not causing massive damage to
exposed populations. The researchers comment:

Bisphenol
A (BPA) is a widely studied typical endocrine-disrupting chemical, and
one of the major new issues is the safe replacement of this commonly
used compound. Bisphenol S (BPS) and bisphenol F (BPF) are already or
are planned to be used as BPA alternatives. With the use of a culture
system that we developed (fetal testis assay [FeTA]), we previously
showed that 10 nmol/L BPA reduces basal testosterone secretion of human
fetal testis explants and that the susceptibility to BPA is at least
100-fold lower in rat and mouse fetal testes. Here, we show that
addition of LH in the FeTA system considerably enhances BPA minimum
effective concentration in mouse and human but not in rat fetal testes.
Then, using the FeTA system without LH (the experimental conditions in
which mouse and human fetal testes are most sensitive to BPA), we found
that, as for BPA, 10 nmol/L BPS or BPF is sufficient to decrease basal
testosterone secretion by human fetal testes with often nonmonotonic
dose-response curves. In fetal mouse testes, the dose-response curves
were mostly monotonic and the minimum effective concentrations were
1,000 nmol/L for BPA and BPF and 100 nmol/L for BPS. Finally,
10,000 nmol/L BPA, BPS, or BPF reduced Insl3 expression in
cultured mouse fetal testes. This is the first report describing BPS and
BPF adverse effects on a physiologic function in humans and rodents.

On a Brighter Note...

While
chemicals like BPA represent a source of great harm, there is plenty of
research revealing that we can mitigate and/or undo some of the damage
associated with its ubiquitous exposure, when eliminating it all
together is not an option. In line with our mission: Education Equal
Empowerment, we have gathered up abstracts from the National Library of
Medicine indicating the in-built resilience of biological systems to
attenuate the adverse effects of these chemicals, such as:

Genistein:
This phytocompound, found in physiologicallly significant
concentrations in soy, red clover and coffee, is capable of reducing the
adverse effect of bisphenol A exposure. Read Studies.

Alpha Lipoic Acid: This compound commonly found in health food stores has been found to mitigate bisphenol A-induced testicular toxicity. Read Study.

Kimchi Probiotics: A bacterial strain in this fermented cabbage extract has been found to degrade bisphenol A. Read Study.

Royal Jelly: Produced by worker bees for the queen, this supernal
elixir has been found also to inhibit the estrogenic and proliferative
(potentially cancer-promoting) effects of bisphenol A. Read Study

Clearly,
the best case scenario is avoiding exposure to bisphenols whenever
possible. However, simply accepting a thermal receipt at a purchase, or
consuming a meal whose ingredients derive from canned foods, makes
avoidance a very difficult proposition. We hope that this research will
foment a movement to pressure manufacturers and regulators to clamp down
on the use of bisphenols.

Sayer Ji is the founder of GreenMedInfo.com, an author, educator, Steering Committee Member of the Global GMO Free Coalition (GGFC), and an advisory board member of the National Health Federation.

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